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This article is written to get you motivated enough to do something as a parent or community leader. The big question: Who's to blame for our current childhood obesity and type 2 diabetes epidemic? Depends on whom you ask. The Institute of Medicine says it's an interaction between genetics and environment. Well, our genetics hasn't changed in 30 years, but our environment has. The body mass index distribution curve shows that all segments of the population are increasing in weight, so whatever's happening is happening to everybody. The U.S. Government calls it a matter of "personal responsibility." How does the 2-year-old population, who is witnessing the greatest increase in prevalence of obesity, accept personal responsibility? The Centers for Disease Control and Prevention says obesity results from an energy imbalance, by eating too many calories and not getting enough physical activity. Big Food says it's a lack of activity, the TV industry says it's the diet. The Atkins people say it's too much carbohydrate, the Ornish people say it's too much fat. The juice people say it's the soda, the soda people say it's the juice. The schools say it's the parents, the parents say it's the schools. How are we going to fix this, when no one will accept responsibility? If you want to just blame American apathy and laxity, all you have to do is look at Japan, China, and France, each of which has witnessed a doubling in the prevalence of childhood obesity in the last 10 years, as well as the rise in prevalence in developing countries in which malnutrition used to be rampant. In other words, it's not Americans; it's humans.

So far, it is just "guilt by association." The not-my-fault two-step has so far succeeded, due to a lack of mechanism, which has allowed each interest group to sidestep their responsibility. So what really has happened in the past 30 years to allow for this? And how did our physiology interact with our environment to create this problem?

The main reason for this conundrum is our casual misinterpretation of the First Law of Thermodynamics, which states: "The energy within a closed system remains constant." In human terms, the First Law is usually interpreted as follows: "If you eat it (energy intake), you better burn it (energy expenditure), or you're going to store it (weight gain)."

There is another equally plausible interpretation of the First Law, which is stated thus: "If you store it, and you expect to burn it, then you have to eat it." In this interpretation, the behaviors of gluttony and sloth become secondary to a pathological process of excess energy storage. Could this instead be what's happening? What is making energy storage go haywire?

To understand dysfunctional energy storage, we must first understand how our body normally regulates energy balance.  Our energy intake vs. expenditure is normally regulated very tightly by the hormone leptin, which transmits the primary controls to the brain for energy balance.

This leptin signal (1) reduces the appetite to decrease further food intake, (2)increases thyroid hormone  and energy expenditure, 3) innervating skeletal muscles to increase energy, and  4) innervating  white adipose tissue to release fat. The magnitude of energy expenditure also increase energy expenditure (eg, caffeine) increase quality of life.

Also leptin causes the brain to reduce the activity of the vagus nerve.  The Vagus increases insulin secretion to increase calories into fat cells, and increases adipose tissue insulin sensitivity to promote energy accumulation in fat.  So when leptin levels are high, the brain senses energy sufficiency, and these vagal energy conserving and storing processes are inhibited.

Every human has a "personal leptin threshold," above which the brain interprets a state of energy sufficiency and the high leptin state is characterized by low appetite, normal physical activity, and feelings of well-being.

Conversely, in conditions of low leptin, such as in the "starvation response," the brain would of  decrease the body’s activity and feelings of well-being, and increase vagal tone to increase appetite and insulin release (to store more energy in adipose tissue). In the energy excess state, humans burn energy at 50 kcal/kg fat-free mass. However, in the starvation state, this is reduced to 40 to 42 kcal/kg fat-free mass.

Obesity is the same process in the brain as starvation. On first thought this sounds ludicrous, but in fact, it actually makes a lot of sense. If you examine the constitutional symptoms of obese and starved individuals, they are similar. Both are associated with fatigue, malaise, lack of activity, inability to motivate, and depression. The reason for this is the ability or inability for the brain to transduce the leptin signal; in starvation because there is inadequacy of leptin, and in obesity because there is resistance to leptin, because it is obviously not doing its job. Furthermore, serum leptin concentrations drop precipitously during periods of short-term fasting (with-in 12 hours), declining faster than body fat stores, which would account for the recidivism of obesity; the hypothalamus is seeing a declining leptin signal similar to starvation, promoting increased energy intake and decreased energy expenditure. Similarly, giving leptin to obese leptin-resistant individuals is not effective.

So what is leptin resistance? And what restores leptin sensitivity? So far, two paradigms for improving leptin sensitivity have been noted.

Forced weight loss.  Rosenbaum employed a 10% weight loss paradigm to induce the starvation response. In these individuals, leptin declined and energy expenditure decreased. However, exogenous administration of leptin in physiologic dosing to approximate the prestarvation leptin level resulted in further weight and fat decrease, along with return of energy expenditure to the prestarvation state. In other words, in the baseline state, subjects were resistant to physiologic concentrations of leptin, while in the weight-reduced state, they were responsive to the same concentrations of exogenous leptin; thus, forced weight loss improved their leptin sensitivity.

We studied children who became obese after brain damage from brain tumors, surgery, or radiation, termed "hypothalamic obesity." Death of these neurons prevents normal leptin signaling, resulting in an "organic leptin resistance," which manifests as a never-ending starvation response and intractable obesity. Hypothalamic obesity is classically unresponsive to diet, exercise, and most pharmacologic manipulations. We treated patients with the somatostatin analog and insulin suppressive agent octreotide. We were able to suppress insulin, stabilize BMI, decrease caloric intake, increase spontaneous physical activity, and improve quality of life commensurate with the degree of insulin suppression. In other words, reduction in insulin reduced hunger, fatigue, malaise, and sloth.

We then treated obese adults (without CNS lesions) with octreotide. We noted significant and progressive BMI loss in about 20% of treated subjects. Recall measurements of caloric intake demonstrated that these responders reduced carbohydrate intake selectively, along with suppression of insulin, while nonresponders did not. In the responders, leptin concentration dropped by 50%, which of necessity should elicit the "starvation response;" despite this, energy expenditure increased in these subjects. We also demonstrated that insulin suppression by octreotide correlated with improved leptin sensitivity.

Rosenbaum through forced weight loss, improved leptin sensitivity as measured by improved energy expenditure in response to leptin. Insulin suppression using octreotide also improved leptin sensitivity, as measured by declining leptin with improved energy expenditure, allowing for weight loss and improved quality of life. Both paradigms share at their core a reduction in insulin concentrations. The similarity of effect between these two paradigms suggest that insulin may be one cause of leptin resistance.

 Insulin Antagonizes Leptin Signaling
Although insulin and leptin bind to separate receptors in the brain, they share the same signaling cascade. It is thought that when insulin levels at the brain are high, then leptin cannot turn on its signaling cascade.

 Adaptive Advantage for insulin as an Endogenous Leptin Antagonist
Teleologically, what could be the biological advantage of insulin antagonism of leptin action in obesity? Leptin is a necessary signal to the brain for the initiation of high-energy processes, such as puberty and pregnancy. If leptin signaling were not modulable, the weight accrual for reproductive competency during puberty and pregnancy would be compromised. Therefore, reversible antagonism of leptin action is in the best interest of our survival. Since insulin causes energy deposition into fat, it makes sense that it should be the central blocker of leptin as well. Indeed, both puberty and pregnancy are hyperinsulinemic and insulin resistant states;  with requisite increases in insulin levels. In both, leptin levels increase slowly, and then when adulthood is reached or post-partum, insulin levels fall, weight stabilizes or is lost, and leptin returns back toward baseline. However, in maladaptive conditions when insulin rises chronically, leptin signaling continues to be impeded, the brain sees starvation, and obesity worsens.

At least three separate reasons for hyperinsulinemia in children can be discerned.

1)      Genetics: children from certain racial and ethnic groups have increased insulin dynamics even prior to the development of obesity, which may predispose them to increased weight gain.

2)      Epigenetics: the "fetal origins of adult disease" hypothesis states that those born small- and large-for-gestational age at birth are prone to developing obesity; both birth weight extremes are states of hyperinsulinemia and insulin resistance, which may worsen beyond the neonatal period.

3)      Our Western environment through three separate submechanisms.

A)    Increased stress with increased cortisol secretion may lead to insulin resistance. Indeed, television watching may in-crease stress levels, increase food intake, foment insulin resistance (as in Cushing's syndrome) and promote obesity.

B)    The loss of daily physical activity due to lack of sidewalks, automobile transport, and screen time (TV, computers, cell phones) foments insulin resistance.

C)    Finally, and most significantly, our current Western food environment is highly insulinogenic, as demonstrated by its increased energy density, high fat content, high glycemic index, increased fructose composition, decreased fiber, and decreased dairy content." In particular, fructose (too much) and fiber (not enough) appear to be cornerstones of the obesity epidemic, through their effects on insulin.

 The most commonly used sweetener in the U.S. diet is the disaccharide sucrose tie, (table sugar), which contains 50% fructose and 50% glucose. However, in North America and many other countries, non-diet soft drinks are sweetened with high-fructose corn syrup (HFCS), which contains up to 55% of the mono-saccharide fructose. Thanks to its abundance, sweetness, and low price, HFCS has become the most common sweetener used in processed foods. It's not that HFCS is biologically more ominous than sucrose; it's that its low cost has made it available to everyone, especially low socioeconomic groups. HFCS is found in processed foods ranging from soft drinks and candy bars to crackers to hot dog buns to ketchup. Average daily fructose consumption has increased by over 25% over the past 30 years. The growing dependence on fructose in the Western diet may be fueling the obesity and type 2 diabetes mellitus epidemics.  Animal models demonstrate that high-fructose diets lead to increased energy intake, decreased resting energy expenditure, excess fat deposition, and insulin resistance, which suggest that fructose consumption is playing a role in the epidemics of insulin resistance and obesity and type 2 diabetes mellitus in humans. The metabolism of fructose differs significantly from glucose. Fructose is absorbed in the intestine and enters the liver without insulin regulation. There, fructose is converted to fructose-1-phosphate and enters the metabolism without regulation. This leads to an excess which cannot be metabolized, and it is then converted into free fatty acids (which promote insulin resistance), very low-density lipoproteins (VLDL, which promote atherogenesis and serve as a substrate for obesity), and triglycerides. Fructose also does not suppress secretion of the so-called "hunger hormone" ghrelin, levels of which correlate with perceived hunger. In sum, fructose consumption has metabolic and hormonal consequences that facilitate development of obesity and its complications. The highest fructose loads are soda (1.7 gm/oz) and juice (1.8 gm/oz).

 Our Western diet also tends to be poor in fiber, which may be one of the characteristics that link it to obesity and insulin resistance. Cohort studies of young and middle-aged adults demonstrate that fiber intake is inversely associated with weight gain, fasting insulin levels, and risk of type 2 diabetes mellitus. Generally, high fiber foods have low energy density. High-fiber meals tend to be more satiating as they induce a greater sensation of fullness than low-fiber meals. Fiber also slows gastric emptying. Fiber-containing foods slow intestinal glucose absorption, which lessens the after-meal  insulin. Why is the Western diet fiber-poor? Because you can't freeze and reheat fiber. Fast food must be shipped to franchises around the world, thus the fiber must be removed first.

This is a difficult proposition,
especially given the current "toxic environment”.   The UCSF Weight Assessment for Tee and Child Health (WATCH) Program advocates four simple rules for treating obesity by bringing the insulin down.

1)      Get rid of every sugared liquid in the house. This means soda, juice, Kool-Aid, sports drinks, etc. Look at the bottle: five calories per serving or less is OK; six or more, leave at the store.

2)      2) Eat your carbohydrates with fiber. White food (bread, rice, pasta, potatoes) is fiberless food. Brown food (brown rice, beans, lentils, peanuts, other legumes) is highfiber food. Alternatively, look at the dietary fiber content: 3 g or more per serving is adequate.

3)      3) Wait 20 minutes for second portions. This takes advantage of another hormone called peptide YY located in the distal intestine, which acts as the satiety signal, preventing that second portion, and further insulin rise.

4)      4) Get the TV out of the kid's room. And kids should buy their TV time minute-for-minute with activity. Since when did TV watching become a child's right?


In this review, the mechanism of our "toxic environment's" effects on insulin and weight gain in the genesis of obesity is elaborated. The composition of our diet is highly insulinogenic. The insulin drives energy into fat, and interferes with leptin signaling in the brain. This results in weight gain and the sense of starvation reducing energy expenditure and physical activity; and increased vagal activity, which promotes yet further insulin release and energy storage. Thus, hyperinsulinemia turns the leptin negative feedback system into a "vicious cycle" of obesity.  Externally, this appears as "gluttony and sloth," but it is biochemically driven.

How does this work? A thin, insulin-sensitive, 13-year-old boy might consume a daily allotment of 2,000 kcal, and burn 2,000 kcal daily (or 50 kcal/kg fat-free mass) in order to remain weight-stable, with a stable leptin level. However, if that same 13-year-old became hyperinsulinemic and/or insulin resistant, perhaps as many as 250 kcal of the daily allotment would be shunted to storage in adipose tissue, promoting a persistent obligate weight gain. Due to the obligate energy storage, he now only has 1,750 kcal per day to burn. The hyperinsulinemia also results in a lower level of leptin signal transduction, conveying a CNS signal of energy insufficiency. The remaining calories available are lower than his energy expenditure; the CNS would sense starvation. He would reduce his physical activity, resulting in decreased quality of life; and through increased vagal tone, he would increase caloric intake and insulin secretion, but now at a much higher level. Thus, the vicious cycle of gluttony, sloth, and obesity is promulgated.

 Is this personal responsibility, when a kid's brain thinks it's starving? Is it personal responsibility when the American Academy of Pediatrics still recommends juice for toddlers? Is it personal responsibility when the Women, Infant and Children program subsidizes fruit juice but not fruit? Is it personal responsibility when the first ingredient in the barbecue sauce is high-fructose corn syrup? Is it personal responsibility when high-fiber fresh produce is unavailable in poor neighborhoods? Is it personal responsibility when the local fast food restaurant is the only neighborhood venue that is clean and air-conditioned? Is it personal responsibility when in order to meet the criteria for No Child Left Behind, the school does away with physical education class? Is it personal responsibility when children are not allowed out of the house to play for fear of crime? We must get the insulin down. Fixing the "toxic environment" by altering the food supply and promoting physical activity for all children can't be done by government, and won't be done by Big Food. This will require a grassroots, bottom-up effort on the part of parents and community leaders.

Adapted from article written by Robert Lustig MD in Pediatric Annals Dec 06


Simple solution for Obesity

 Here are some simple guidelines for diet and exercise I would like to share with you.

Eat only 6 things for breakfast, lunch and dinner:

- Fruits

- Grains and Vegetables (careful with corn and potatoes)

- Meat

- Chicken (turkey ok)

- Fish

- Eggs 

Big breakfast, medium lunch, small dinner. Nothing after 6 pm except water.

No fast food. Eat half of what restaurants give you.

Do not eat anything that comes in a box.

No white foods (bread,starches,corn,pasta,rice).

This provides carbs in their natural form. This is how our great-great-great-great grandparents ate. You can give alternatives: corn tortillas, brown rice, whole grain bread

The catch is that carb addiction is almost an "all or none" phenomenon. If someone is dieting but decides to have a piece of cake, this transitory hyperglycemia will release endorphins that will require his/her body to "ask" for more.

Use a pedometer and get at least 10,000 steps daily. Limit the video games and TV.  Get those teens one of those dance revolution video game dance pads-- that will help them break a sweat....

Drink  8-10 glasses/day only water or diet drinks.  No regular sodas or fruit juices. Teenagers are consuming 1000+ calories (mostly carbs) in the form of drinks (gatorade, kool aid, sodas, etc). When your fluid intake is only water then you cut down 1000+ cal/day. That is 1 pound in 3 days only from drinks.

 Sometimes we are thirsty instead of hungry. When we drink water we cut some cravings. Water also helps constipation. It flushes your toxins.   Also you may have an acid heartburn stomach feeling and think that you are hungry.  Take an antacid with the water and that can help that craving.

On this diet kids can lose 10 lbs/ month and so are their parents.  Diets work if the whole family participate. It's not about dieting for short term results, rather lifestyle change for sustained improvement in health ... every day the rest of your life.

 You can cut back eating for one week and loose 1 lb and eat too much for just one day and put 1 lb back on.  So people think they starve all the time and not loose weight because they forget about the one day they ate too much.  You change your way of eating every day!

 Loosing weight is like a marathon race.  You don’t run the first mile as fast as you can go or else you get tired too soon and stop running.  If you try to loose too much weight too fast, then you will get exhausted and quit.  Cut back the calories so you are loosing it 1-2 lb a week.  It will take a long time to get your weight down but since we are going to change the way we eat for the rest of our lives…. Then it does not matter how long it takes.

Studies showed that snacking was not as important contributor of over weight as was fast food.  So eating at home helps (family meals are very important), keep low portion sizes, and no sweet drinks.


Calories in common drinks. snacks. and fast food:

Type                                Source                                Item                                                Calories

www.coca-cola.com       20 oz Coke       250

                                www.pepsi.com                                20 oz Pepsi                                250

                                www.starbucks.com                                 16 oz (Grande) Caffe Latte                                 260

                                                                                                          20 oz (Venti) Caffe Latte                                 340

                                                                                                           16 oz Caffe Mocha                                300

                                                                                                            With whipped cream                                400

                                                                                                            20 oz Caffe Mocha                                390

                                                                                                            With whipped cream                                490

                                www.orangejulius.com                             20 oz original Orange Julius                                 270

                                                                                                             32 oz original Orange Julius                                 440                         

                                                                                                            20 oz BlackBerry Storm Smoothie                                630

Snacks                    www.calorie-count.com                                Candy bar; Snickers and Hershey's                                200-300

                                www.fritolay.com                                1 oz bag of Lays Classic Potato Chips (20 chips)      150

                                                                1 oz bag of Doritos NACHO CHEESE' Flavored                                140

                                                                1 oz bag of Fritos Corn Chips (32 chips)                                160

Burgers                                www.mcdonalds.com                                McDonald's Hamburger                                250

                                                                                                                With cheese                                300

                                                                                                                McDonald's Quarter Pounder`"                                410

                                                                                                                With cheese                                510

                                                                                    McDonald's Big Mac                                540

                                www.bk.com                                                Burger King Original Whopper"','                                670

                                                                                                                With cheese                                760

Chicken                   www.kfc.com                                                One Original Recipe chicken drumstick                                130

                                                                                                                One Original Recipe chicken breast                                360

French Fries          www.mcdonalds.com                                         McDonald's small fries                                 250

                                                                                                                   McDonald's medium fries                                 380

                                                                                                                    McDonald's large fries                                570

                                www.bk.com                                                     Burger King small fries                                 230

                                                                                                                    Burger King medium fries                                 360

                                                                                                                    Burger King large fries                                 500

                                                                                        Burger King King-sized fries                                600

Pizza                                www.dominos.com                                1 slice of a Domino's 14" cheese pizza                                220

                                                                                                                    1 slice of a Domino's 14" pepperoni pizza                                270

                                www.papajohns.com                    1 slice of a Papa John's 14" cheese Pizzza                                300

                                                                                                1 slice of a Papa John's 14" pepperoni pizza                                310

                                www.pizzahut.com                        1 slice of a Pizza Hut 14" cheese pizza                                390

                                                                                                    1 slice of a Pizza Hut 14" pepperoni pizza                                400


Many restaurants will have a Web site that will list nutritional information for their menu items. Web sites can be found by putting the name of the franchise into a search engine such as www.google.com Other Web sites that list calories in common foods include www.dietfacts.com, www.calorie-count.com, and http://weightlossinternational.com/newsletter/free-online-calorie-counter.html